Electronic fetal monitoring

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Electronic Fetal Monitoring
Workshop
2016
By
Ahmed Elbohoty MD, MRCOG
Assistant professor of obstetrics and gynecology
Ain Shams University
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Learning Objectives
• By the end of this day, every candidate should
have been able to:
1. Appreciate the importance of intrapartum fetal heart rate monitoring
2. Understand the pathophysiology of fetal hypoxia
3. Understand the indications and the limitations of the EFM during the
intrapartum period.
4. Understand the components of the trace with the significance of each
part.
5. Interpret cardiotocographic (CTG) abnormalities that might suggest
hypoxia
6. Interpret the trace of EFM in line with the clinical scenario of the case.
7. Perform the suitable actions according to the global evaluation, not only
to the recorded trace.
8. Determine the role of fetal scalp blood sampling
9. Improve your decision making in intrapartum management2/29/20 ELBOHOTY 3
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The rationale for EFM
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Introduction
• Intrapartum (IP) hypoxia occurs in about 1% of
labours and can cause fetal/neonatal death and
disability.
• A cardiotocograph (CTG) has a high false positive
rate when interpretation is solely based on pattern
recognition.
• Understanding the control of fetal heart rate and
the pathophysiology of hypoxia helps to interpret
CTG traces and institute appropriate measures to
improve fetal outcome.
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Does EFM protect babies from any harm?
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Cochrane systematic review
• In low-risk labouring women:
• Compared to intermittent auscultation (IA),
continuous EFM showed no difference in overall
perinatal death rate
• Compared to intermittent auscultation (IA),
continuous EFM was associated with a halving of
neonatal seizures but had no significant difference
in reducing subsequent cerebral palsy
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Does the same apply to high risk
labours?
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Since the introduction of EFM
• The incidence of HIE and perinatal death related
to fetal hypoxia has fallen In addition, in that
time, caesarean section rates have risen
significantly.
• Published data clearly indicate that the incidence
of the three main complications of IP fetal
hypoxia are falling (rates are per 1000 total
births):
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Evidence for falling incidence of
complications due to intrapartum fetal hypoxia
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Hypoxic ischaemic encephalopathy (HIE)
Smith J, Wells L, Dodd K. The continuing fall in incidence of hypoxic-ischaemic encephalopathy in term
infants. BJOG: An International Journal of Obstetrics & Gynaecology 2000;107:461-466.
Strijbis EM, Oudman I, van Essen P et al. Cerebral palsy and the application of the international criteria for
acute intrapartum hypoxia. Obstet Gynecol 2006;107:1357-1365.
Percent of cerebral palsy cases
due to IP fetal hypoxia
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Medicolegal Aspects
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• The NHS Litigation Authority (NHSLA) is a
government department established to deal with
litigation in the NHS.
• Obstetrics is not numerically the most frequent
offender in terms of medicolegal cases. However,
financially it results in a huge drain of resources.
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• The reason for this is clear to all who practise
obstetrics; the financial payout to support children
with brain damage caused by problems that occur
in labour are substantially greater than those that
result in death.
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Medicolegal issue
• The 4th Confidential Enquiry into Stillbirths and Deaths
in Infancy (CESDI) in 1995, highlighted intrapartum
deaths and the difficulties that arise with electronic
fetal monitoring.
• Nearly 50% of the 800 intrapartum deaths were
attributed to:
– a failure to recognise the CTG trace abnormalities
– a delay in communication and timely action
– a combination of these.
• Only 21% of the claims involved high-risk pregnancies,
indicating the importance of the effective monitoring of
all women.2/29/20 ELBOHOTY 15
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• Hypoxic brain injury or death of the fetus accounts for
nearly 38% of claims handled by the Medical Defense
Union and Medical Protection Society in the UK.
• Nearly £200million was paid out in 1998 in claims
related to obstetrics, largely for birth asphyxia.
• From 1995 to the end of March 2011 there were 13
000 claims for obstetrics and gynaecology, the
estimated value of which was more than £5.2 billion.
• From 2000 to 2010 there were 5087 maternity claims,
the total value of which was £3,117,649,888.
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Misinterpretation of CTG is still one of the major reasons for a huge number of claims
received by the NHS Litigation Authority (NHSLA), along with delay in acting on an
abnormal CTG.
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Record keeping
• Keep cardiotocograph traces for 25 years and, if
possible, store them electronically.
• In cases where there is concern that the baby may
experience developmental delay, photocopy
cardiotocograph traces and store them indenitely in
case of possible adverse outcomes.
• Ensure that tracer systems are available for all
cardiotocograph traces if stored separately from the
woman's records.
• Develop tracer systems to ensure that cardiotocograph
traces removed for any purpose (such as risk
management or for teaching purposes) can always be
located.2/29/20 ELBOHOTY 18
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Basic pathophysiology of FHR
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Contents
Physiological Control of fetal heart rate
Pathogenesis of fetal hypoxia
Fetal response to hypoxia
Fetal response to normal labour
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Fetal heart rate with GA
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• As early as 6 weeks menstrual age (4 weeks post conception):
• The fetal heart is detectable by transvaginal US
• The mean FHR is about 100 bpm.
• At 10 weeks menstrual age (8 weeks post conception):
• it progressively rises, reaching a mean of about
140-150 by14 weeks
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• From 14 weeks menstrual age to term:
• there is a progressive fall in the mean baseline FHR
• This lowering of the baseline rate with gestation is a
reflection of the fact that the sympathetic autonomic
nervous system matures earlier than the parasympathetic.
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Physiological control of FHR
Intrinsic
Extrinsic
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• Dominant pacemaker activity of the sinoatrial node
in the atrium
Intrinsic
Early in the second trimester, the average baseline
fetal heart rate is about 160 beats per minute
(bpm).
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Extrinsic
Nervous
Hormonal
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Autonomic nervous system (extrinsic)
• Sympathetic (noradrenergic)
• Parasymathatic (cholinergic)
• They can control heart rate and variability
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Early deceleration
• Head compression is
associated with activation
of the parasympathetic
nervous system and hence
result in early deceleration
with uterine contraction.
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Catecholamines
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Baroreceptor and Chemoreceptor
Reflexes
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Effect of ANS on fetal HR
• Baseline variability
• A moment-to-moment
or beat-to-beat
oscillation of the
baseline heart rate.
• This is produced by a
sympathetic push and
parasympathetic pull on
the sinoatrial node.
• Heart rate
• Parasympathatic
reduces the HR
• Symathatic increases
the HR
Sympathatic development matures earlier than parasympathatic
Extreme Prematurity (GA less than 28 weeks) is associated with baseline tachycaria and
decreased variability.
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But other factors also influence the FHR patterns, including:
1. fetal activity state
2. medication
3. infection
4. chromosomal and central nervous system abnormalities
5. congenital or intrauterine infection
6. fetal anaemia
7. fetal cerebral haemorrhage
8. head compression.
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Variation in the baseline variability
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• The baseline variability of the FHR in early pregnancy is low and
increases with gestation, but that is refined by the behavioural state of
the fetus.
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• Over the second half of pregnancy the baseline
variability increases progressively during fetal activity
• At 30 weeks there is not much difference in baseline
variability between fetal activity and quiescence.
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• By 38 weeks when the fetus is quiet the baseline
variability is very low (with a ‘flat’ trace) and in
activity the baseline variability is greater.
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Cycling
• Periods of activity and quiescence and reflects an
intact and functioning central nervous system.
• The CTG opposite shows a period of quiescence
followed by activity which is a hallmark of fetal
wellbeing.
• The presence of a stable baseline FHR and a
reassuring baseline variability denote non-
depressed autonomic nervous system centres
(sympathetic and parasympathetic).
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Types of Variability
•Short-term variability reflects the
instantaneous change in fetal heart
rate from one beat—or R wave—to
the next. It can most reliably be
determined by fetal ECG.
•Long-term variability is used to
describe the oscillatory changes that
occur during the course of 1 minute
and result in the waviness of the
baseline
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Acceleration
• FHR is increased by fetal activity in utero, which is
mediated through the fetal somatic nervous
system
• It increases in height as gestation advances
• Accelerations are considered as hallmarks of fetal
wellbeing
• A sick or hypoxic fetus would reduce its
movements to conserve energy and therefore is
unlikely to show accelerations on the CTG.
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Baroreceptors
• Site: carotid sinus and aortic
arch
• Trigger: changes in arterial
blood pressure.
• Effects: Stimulation by
increased blood pressure
leads to activation of the
parasympathetic nervous
system that results in a fall in
the FHR.
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• This will be visible as a deceleration on the CTG.
• Such a deceleration is usually short-lasting and rapidly
returns to the baseline heart rate as it is a reflex
neurological mechanism.
• Head compression and true cord compressions are
associated with activation of the parasympathetic nervous
system and hence result in early and variable
decelerations respectively, both of which are short-lasting.
• The fetus is not exposed to hypoxia during these
decelerations (as they are due to mechanical
compression), so they do not warrant any intervention.
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Variable deceleration
• mechanical compression on the umblical cord
leads to:
1. the thin-walled vein becomes occluded first
• The decreased venous return to the heart
precipitates a transient reflex tachycardia that is
seen as the initial
2. If the pressure on the cord becomes greater,
the small, thick-walled umbilical arteries also
become compressed.
• a rapid increase in fetal blood pressure that
activates a fetal baroreceptor-reflex response.
• Vagal stimulation occurs, and the FHR decreases
abruptly.
3. Once compression of the umbilical cord is
relieved, the higher elastic arteries open first,
but the umbilical vein still may be compressed.
• A transient tachycardia (posterior shoulder) may
occur.
4. As perfusion in the umbilical vein resumes
• the blood pressure normalizes and the FHR returns
to baseline.
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Chemoreceptors
• Sites:
– Peripheral chemoreceptors are located on the aortic and
carotic bodies
– Central chemoreceptors are situated within the brain.
• Trigger: Increased carbon dioxide and hydrogen ion
concentration coupled with decreased oxygen
content of the fetal blood stimulate the
chemoreceptors
• Effects:
• Ealry: increase the release of catcholamines which causes tachycardia and
vasoconstriction
• Late or sustained: This results in activation of the parasympathetic centre in
the brain, leading to a fall in the FHR.
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Late decelerations
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• They are considered ominous as they
are likely to reflect a chemoreceptor-
mediated fall in the FHR.
• Unlike the baroreceptor-mediated
deceleration, the chemoreceptor-
mediated deceleration takes a longer
time to recover to the normal baseline.
• because fresh maternal blood is
required to 'wash-out' the accumulated
acid and carbon dioxide, which takes
time, leading to a 'lag time'.
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The importance of oxygen
• Aerobic respiration with production of
– high ATP 32-38 molecule
– CO2
– H2O
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The physiological advantages of
1. high fetal haemoglobin concentration
2. increased affinity of fetal haemoglobin for oxygen
These makes the fetus relatively resistant to mild to moderate
hypoxia.
How can the fetus ensure delivery of the
O2 from the mother?
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Hypoxemia
sO2
Hypoxia
Asphyxia
Consequences of impaired fetal
oxygenation
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• 1. Hypoxaemia
A reduction in oxygen carried in the blood
as a result of decreased pO2 and
decreased oxygen content.
Compensation:
• Increased oxygen extraction.
• Chemoreceptors are stimulated
• Release of catecholamines
• Redistribution of blood flow
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• 2. Hypoxia
• Oxygen supply is insufficient for tissue energy by
aerobic pathway
• Compensation:
• Surge of stress hormones
• Redistribution of blood flow
• Anaerobic Glycolysis becomes more active to
maintain energy balance
• Only 2 ATP
• lactic acid
• However, buffers act to resist any pH changes.
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• 3. Asphyxia
• Continuing hypoxia leads to
– Predominance of anaerobic metabolism and production
of lactate and hydrogen ions is beyond the buffer
system which leads to acidosis.
– Energy balance will no longer be maintained
– Organ damage can occur
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Cardiovascular response
• The fetal response to hypoxia differs in individual
cases, depending on
– fetal reserve, antenatal and intrapartum risk factors.
some individual variation in the capacity to react to
hypoxia/acidosis.
– The severity and rapidity of insult
• In some cases, there may be a sudden and almost total
reduction in oxygen supply, while in others,
• it may be less intense or of slower onset.
• The insults can also be transitory and repetitive in nature
(uterine hypercontractility, occult cord compression).
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Sequence of fetal response to hypoxia
Sympathetic stimulation to increase catecholamine levels, which first
increase heart rate
Fetal movement is abolished so that accelerations of the FHR
disappear
Variability may also start to decrease.
Cathecolamines constrict peripheral arterial beds, resulting in systemic
hypertension which stimulates Baroreceptors with subsequent slowing
of the fetal heart related especialy related to uterine contractions
Further hypoxia stimulates chemoreceptors resulting in vagal
stimulation with bradycardia.
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Fetal hypoxia
1. CTG changes could be the sign of hypoxia.
2. It may not always be due to hypoxia,other factors
such as infections ,medications,maternal
position,can cause changes to CTG.
3. CHECK AND CORRECT
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Long-standing (or 'chronic') hypoxia
utero-placental insufficiency
reduced pO2 to fetal CNS
redistribution of fetal cardiac output
perfusion to CNS & heart perfusion to peripheral & viscera
renal perfusion visceral circulation
OLIGOHYDRAMNIOS
bowel distension umbilical arterial resistance
meconium peritonitis
necrotising enterocolitis etc
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Events in Asymmetrical SGA
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September 2014/March
2015
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Long-standing (or 'chronic') hypoxia
• Causes:
– Presence of FGR
– Infection
– antepartum haemorrhage
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CTG
• Tachycardia
• variability is less than 5 bpm (usually <2 bpm) with shallow
decelerations less than 15 beats.
• With the contractions of labour, there may be sudden bradycardia
and fetal death within a relatively short time (1–2 hours).
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Acute hypoxic event
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• Acute hypoxic insults can cause hypoxia in
previously uncompromised fetuses.
• The CTG may have been normal until the onset of
the insult.
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Causes
– Cord prolapse
– Uterine rupture (which can occur in an unscarred uterus)
– Placental abruption
– Maternal hypotension
– Hyperstimulation
• Some fetuses develop acute hypoxia in labour
without any clear precipitating cause, and the
absence of an apparent mechanism does not
exclude acute hypoxia.
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Main causes of acute fetal hypoxia/acidosis
• Reversible causes
– Uterine hypercontractility
– Sudden maternal hypotension
– Maternal supine position with aortocaval compression
• Irreversible causes
– Major placental abruption
– Uterine rupture
– Umbilical cord prolapse
• Maternal cardiorespiratory disorders
– Severe asthma, haemorrhagic shock, cardiorespiratory arrest,
pulmonary thromboembolism, amniotic fluid embolism, generalised
seizures, etc.
• Usually occult causes
– Occult cord compression (true cord knot, low-lying cord, nuchal cord with
stretching) Major fetal haemorrhage (fetal-maternal haemorrhage, ruptured vasa
praevia)
• Specific mechanical complications of labour
– Shoulder dystocia
– Retention of the after-coming head2/29/20 ELBOHOTY 62
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Acute hypoxia results in a sudden drop
in baseline FHR.
• It has 3 types
• Single prolonged deceleration where the acute hypoxia lasts
for less than three minutes and then recovers to normal
baseline
• Prolonged decelerations lasting for more than three minutes
• Prolonged baseline bradycardia where the FHR remains below
100 bpm (80 bpm in severe cases of hypoxia) for over 10
minutes
• In the presence of acute hypoxia, the fetal pH has
been shown to drop at the rate of 0.01/minute.
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Late
Deceleration
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Prolonged acidosis results in acidosis which causes
persistent bradycardia or repetitive late
decelerations related to myocardial depression.
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O2 level also drops
Heart rate further slows down
Fetal response to acute
Hypoxia
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Subacute hypoxia
• In this situation, the fetus spends more time
decelerating and progressively less time at the
normal baseline FHR.
• Typically, the fetus spends less than 30 seconds at
the baseline to 'wash off' carbon dioxide and acid
and spends over 90 seconds building up carbon
dioxide and acid.
• The pH of the fetus has been shown to drop at the
rate of 0.01 every 2-3 minutes.
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Sequence of events
• Hypoxic stress may develop over hours rather than minutes
during labour and this may provide the fetus with the
opportunity to utilise its compensatory mechanisms to avoid
hypoxic injury.
• In this scenario, the CTG would initially show decelerations
followed by the disappearance of accelerations as the fetus
attempts to conserve energy by limiting muscle activity that
may increase its oxygen requirement.
• If the hypoxic insult continues, the fetus then releases
catecholamines to increase the heart rate and its cardiac
output to supply vital organs.
• The CTG opposite shows gradually-evolving hypoxia. Note the
decelerations (hypoxic stress) followed by a rise in baseline
heart rate (due to release of adrenaline/noradrenaline from
the adrenal glands).2/29/20 ELBOHOTY 69
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• With both long-standing hypoxia and pre-terminal CTG
traces, the fetus has exhausted all its reserves or is
unable to compensate (e.g. due to intrauterine growth
restriction).
• In the former, the hypoxic insult has occurred at some
point during the antenatal period (i.e. prior to the
onset of labour) and the CTG often shows a higher
baseline with reduced variability and shallow
decelerations with uterine contractions.
• Such uterine contractions during labour may cause
further episodes of hypoxia and hence may worsen the
existing cerebral damage.
• Prolonged bradycardia as well as total loss of variability
(often with shallow decelerations) are often referred to
as a pre-terminal CTG; in such cases, the fetus requires
immediate delivery.
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overshoot
• Increase in the reactive tachycardia (or 'shoulder') that
follows a variable deceleration is called an overshoot.
• This should be considered as a pre-pathological feature since
scientific studies have confirmed that such overshoots occur
due to fetal hypotension.
• Persistent falls in fetal mean arterial blood pressure result in
attempts at fetal compensation, which in turn result in such
transient tachycardia or overshoots.
• Overshoots occur due to recurrent and prolonged episodes of
umbilical cord compression and are often seen during
– the second stage of labour
– during oxytocin augmentation; that are characterised by repeated
and strong uterine contraction and the resultant umbilical cord
compression.
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Decelerations with overshoots
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Gradually developing hypoxia in labour can
be due to:
• Repeated episodes of occlusion of the umbilical
cord (suggested by variable decelerations)
• Inadequate intervillous pool of blood (placental
reserve) due either to reduced uterine or placental
perfusion
• Inadequate placental function for exchange to occur
during a contraction (suggested by late
decelerations, due to either chronic uteroplacental
disease or placental abruption)
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Stress pattern
• Cord compression can lead to nonreassuring
variable decelerations.
• In a fetal heart rate trace that was previously
reactive, the presence of these decelerations
without a rise in baseline rate or reduction in
baseline variability is called ‘stress pattern’.
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Stress to distress pattern
1. When hypoxia develops gradually, one of the first
features to be noted is:
• the absence of accelerations.
2. If the oxygen requirement is not met, absence of
accelerations is followed by
• a rise in the baseline rate up to the possible maximum.
3. This in turn is followed by
• a reduction in baseline variability, possibly due to hypoxia of
the autonomic nervous system.
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Distress to death pattern
• In the absence of timely intervention, the fetus may
reach the 'distress platform' of its own
– maximal tachycardia with no accelerations and marked
reduction in baseline variability of less than five beats
per minute.
• It may then be born with hypoxia and acidosis.
• If the situation is ignored the fetal heart rate may
suddenly decline in a stepwise manner leading to
– terminal bradycardia.
• This period is termed distress to death interval and
is usually short (20-60 minutes) once the fetal heart
rate starts to decrease.2/29/20 ELBOHOTY 78
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Adverse Fetal Outcomes
• Severe acidaemia (pH<7.0) is associated with an
increased risk of neonatal death.
• Acidosis (low pH) together with an abnormal base
excess and bicarbonate level predicts the risk of
hypoxic ischaemic encephalopathy (HIE) better than
pH alone.
• A fetus with a base excess <-20 mmol/L is at a more
significant risk of seizures and HIE, while a fetus
with a base excess of -12 mmol/L or less is at
increased risk of admission to intensive care.
• Acidaemia is less likely (<1%), if there is an
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CP and intrapartum hypoxia
• The origins of many cases of cerebral palsy are
antenatal.
• There are seven criteria that should ideally be met
for a case of cerebral palsy to be causally linked to
acute intrapartum hypoxia.
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The two most specific are:
1. Evidence of metabolic acidosis in intrapartum umbilical
cord at arterial or very early neonatal sample(pH<7 and
base deficit >12 mmol/L)
2. Early onset severe or moderate neonatal
encephalopathy in infants of greater than 34 weeks of
gestation. Cerebral palsy of the spastic quadriplegic or
dyskinetic type
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Criteria that together suggest intrapartum
timing but by themselves are non-specific
are:
1. A sentinel hypoxic event occurring immediately before
or during labour
2. Apgar scores of 0-6 for longer than 5 minutes
3. A sudden rapid and sustained deterioration of the fetal
heart rate pattern usually after the hypoxic sentinel
event where the pattern was previously normal
4. Early evidence of a multi-system involvement
5. Early imaging evidence of acute cerebral abnormalities
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What is your judgment about this CTG
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• This CTG shows absent variability with
decelerations, which may indicate impending
fetal demise
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Is Normal labour dangerous to the fetus?
91
The Fetus during Labour
• Labour is a very stressful period for the fetus
• The intrauterine environment dramatically changes
within a short period of time.
• The uterine walls that have been quiescent to allow
the growth of the fetus during pregnancy suddenly
commence contracting strongly and 'squeeze' the
baby approximately 3-4 times every ten minutes,
each contraction lasting for 40-60 seconds.
• The umbilical cord that is essential for oxygenation
and removal of waste products as well as the fetal
head are likely to get compressed during
contractions.2/29/20 ELBOHOTY 92
92

2/29/20
ELBOHOTY47
• Each uterine contraction is associated
with a temporary reduction of placental
blood flow and placental oxygen
exchange.
• The healthy fetus has enough metabolic
reserves to be able to cope with these
periods of hypoxia for hours during
labour.
• Between contractions, uterine perfusion
normalises and placental oxygen
exchange resumes.
Effects of labour
2/29/20 ELBOHOTY 93
93
Fetal oxygenation is therefore dependent
upon many factors in this process.
Anything that disturbs this chain of oxygen
transfer will potentially affect fetal
oxygenation and the FHR. The key
components of the chain are:
•Maternal blood pressure and
oxygenation
•The integrity of the placenta,
specifically the amount of surface area
for oxygen transfer
•The patency of the umbilical cord
Other factors
2/29/20 ELBOHOTY 94
94

2/29/20
ELBOHOTY48
Fetal compression and variable degrees of hypoxia
stimulate increased production of fetal
catecholamines (4x greater than babies born by
caesarean section).
This is an adaptive response to extra-uterine life:
1. stimulates breathing
2. increases fluid absorption in the lungs
3. stimulates surfactant release
4. mobilises glucose and fatty acids
Fetal responses to labour
2/29/20 ELBOHOTY 95
95
Fetal response to stress
• A fetus may demonstrate an alarm reaction by
releasing catecholamines from the adrenal glands
to cope with this stress, just like adults facing a
stressful situation.
• Hence, fetal heart rate (FHR) is likely to show
changes as a result of these mechanical stresses,
which will be recorded in the CTG trace.
• However, the fetus does not require any
intervention as it is a physiological response to
stress.
2/29/20 ELBOHOTY 96
96

2/29/20
ELBOHOTY49
Coping with the stress
• It is important to appreciate that the ability of the fetus
to mount a successful alarm reaction to cope with the
hypoxic or mechanical stress during labour would
depend on the physiological reserve of the fetus.
– A preterm, posterm or fetus with intrauterine growth
restriction may have reduced utero-placental reserve as well
as its inherent physiological mechanisms to withstand
hypoxic stress.
– The rapidity of development of hypoxic stress (i.e. the time
available for the fetus to defend itself through the release of
catecholamines)
– Other clinical factors, such as the presence of meconium or
infection (fetal infection decreases the ability to mount a
successful response and also may potentiate the detrimental
effects of hypoxia on the fetal brain), also play a key role in
this.2/29/20 ELBOHOTY 97
97
How does hypoxia affects the outcome?
2/29/20 ELBOHOTY 98
98

2/29/20
ELBOHOTY50
Behavior patterns
2/29/20 ELBOHOTY 99
99
• Over the last trimester the normal fetus commonly
manifests three behavioural states defined on the basis
of three parameters
– FHR (1F)
– Eye movements (2F)
– Body/limb movements (4F)
• The nomenclature is derived from the five behavioural
states manifest by newborns.
• Change from one behavioural state to another is
accomplished within 3 minutes.
• The time characteristics of the three behavioural states
differ
• These are important physiological developments which
should be born in mind when interpreting FHR
recordings.2/29/20 ELBOHOTY 100
100

2/29/20
ELBOHOTY51
2/29/20 ELBOHOTY 101
101
the FHR (1F)
Low variability baseline FHR, no eye movements, occasional ‘startle’ body
movement with brief rise in FHR, present on average for ~30% of the time,
maximum duration <40 min (can be longer but this is a reasonable definition
for use in practice).
Danger. This pattern can be misinterpreted as a pathological
unreactive FHR trace.
102

2/29/20
ELBOHOTY52
Eye movements (2F)
High variability baseline FHR, eye movements,
many fetal movements with FHR accelerations,
present on average for ~60% of the time,
maximum duration >90 min.
103
Body/limb movements (4F)
Sustained accelerations with occasional return to baseline FHR, eye
movements, continuous fetal movements, present on average for ~10% of
the time, maximum duration >120 min.
Danger. This pattern can be misinterpreted as a baseline fetal
tachycardia with the returns to a normal baseline wrongly called
decelerations.
104

2/29/20
ELBOHOTY53
105
Body
movements
Eye
movements
+ +Active sleep
--
CTG
Deep sleep
+++ +Active awakeness
• Cycling represents the hallmark of neurological responsiveness
• Transitions become clearer > 32-34 weeks
• Deep sleep may last 50 min
Behavioural states
106

2/29/20
ELBOHOTY54
Interpretation of CTG
107
The carditocogram
• A continuous recording
of the fetal heart and
uterine contractions
108

2/29/20
ELBOHOTY55
109
Components of CTG
• FHR is picked up by an transducer placed on the
maternal abdomen (or by an electrode attached to the
fetal scalp) and works by use of Doppler technology.
• The resultant returning sound waves are recorded on a
paper, similar to an adult electrocardiograph (ECG). This
forms the 'cardiac' part of the fetal CTG.
• The usual paper speed in the UK is 1 cm/minute.
• Another electrode is placed on the maternal abdomen
to record the frequency and duration of the uterine
contractions and this forms the 'toco' part of the fetal
CTG.
110

2/29/20
ELBOHOTY56
The ultrasound probe transmits the
fetal heart rate in beats per minute.
The pressure transducer
transmits the pressure generated
by uterine contractions in mm Hg.
•Each small vertical square is 5 mm
Hg
Pressure Transducer
Ultrasound Probe
External monitor
111
Internal Monitoring
Spiral Electrode is placed on the fetal occiput
It is not affected by maternal or fetal movement
as with external monitoring.
Criteria for Internal Monitoring:
§ Amniotic membranes must be ruptured
§ Cervix dilated at least 2 cm.
§ Presenting part down against the
cervix
Not suitable with any contraindications of FBS
112

2/29/20
ELBOHOTY57
Application of the fetal scalp electrode
• Avoid large areas of caput.
• Hold the plastic guide firmly against the scalp and
rotate
• the FSE through at least 1¼ clockwise rotation, until
resistance is felt on gentle traction.
• Check the FSE is not attached to maternal tissue.
• Wipe the end with an alcohol cloth to remove any
liquor etc, and then attach to the skin electrode.
113
Attached spiral electrode with the guide tube removed.
114

2/29/20
ELBOHOTY58
Antenatal vs. Intrapartum
• First of all, we should differentiate between:
– antenatal electronic fetal monitoring (EFM) which is
termed non-stress test (NST)
– intrapartum EFM, which is termed intrapartum
cardiotocography (CTG).
115
Clinical Significance of Antenatal NST
• Analysis of 13 trials of NST has failed to demonstrate any
significant effect on perinatal outcome on low risk
labouring women.
• In a systematic review of 4 RCTs , NST was associated with a
trend towards increased perinatal mortality. This may be
mainly related to unnecessary premature interventions
based on falsely abnormal NST.
• Therefore, NST should only be applied when indicated,
and cautiously interpreted in context with the overall
clinical scenario.2/29/20 ELBOHOTY 116
116

2/29/20
ELBOHOTY59
Interpretation of the Antenatal
NST
117
Classification of Antenatal NST
• Normal NST: a NST with all features reassuring.
• Abnormal NST: a NST with one non-reassuring
feature.
Accelerations should be present =/> 2 episodes in 20mins,
each being at least 15bpm above the baseline rate lasting
for =/> 15 seconds. In an antenatal CTG
118

2/29/20
ELBOHOTY60
Antenatal
NST Reassuring Non-Reassuring
Baseline rate 110 – 160 bpm •100 – 109 bpm
•161 – 180 bpm
Comments:
Variability 5 bpm or more < 5 bpm for 30 min Comments:
Accelerations present Comments:
Decelerations None •Unprovoked decelerations.
•Decelerations related to uterine
tightening (not in labor)
Comments:
Opinion
Normal NST
(all 4 features reassuring)
Abnormal NST
(one or more of the non-reassuring
features)
Maternal Pulse Membranes ruptured: Y/N
State date and time if Yes
Liquor Color Gestational Age
Reason for NST
Action
Date:
Time:
Signature: Status:
119
Computerized
CTG:
The Dawes
Redman CTG
analysis
Criteria met: The Dawes/Redman criteria can meet
the criteria as early as 10mins
if the criteria is met at this point
the CTG can be considered
normal and discontinued
it does not need to continue for
the traditional 20 minutes.
It is valid for any gestation over 26 weeks but it is
not suitable for intrapartum CTG analysis.
It can be used for antenatal CTG, priority should be
given to cases where there is concern about fetal
wellbeing, e.g. SGA with abnormal Doppler’s.
120

2/29/20
ELBOHOTY61
Criteria
not met
If the criteria are not met it must be continued
for 60 minutes, at this point the CTG should
be discontinued and an appropriate clinical
review/action must be taken.
There will be specific reason codes as to why
the criteria have not been met.
The STV should be taken into account and the
trend reviewed if previous analysis has been
performed.
A low STV is most commonly associated with
growth retarded, chronically stressed fetuses.
2/29/20 ELBOHOTY
121
STV values:
normal low Abnormal Highly abnormal
≥4 <4 <3 <2
STV is recorded on the CTG when Dawes-Redman criteria is not met; this
is the best predictor of fetal wellbeing
• Valid only when measured after 60 min of CTG monitoring
• STV >4.0: hypoxia is unlikely
• >37 weeks’ gestation: repeat CTG later the same day
• <37 weeks’ gestation: repeat CTG the following day
• If fetal movements reduced, contact medical staff – CTG to be
repeated later the same day
• STV 3.0–3.99: repeat CTG ≤4 hr and notify middle grade obstetrician
(ST3–7 or equivalent e.g. staff grade, clinical fellow)
• If STV <3.0: pre-terminal trace – notify medical staff immediately
• For SGA with lost or reversed diastolic flow: Use cCTG when DV
Doppler is unavailable or results are inconsistent – recommend
delivery if STV < 3 ms
122

2/29/20
ELBOHOTY62
Intrapartum fetal monitoring
123
Simple measures can help to avoid hypoxia include:
1. Avoiding supine hypotension
2. Avoiding hyperstimulation by judicious use of oxytocin
3. Careful assessment of risk factors at the onset of labour
4. A high index of clinical vigilance and early intervention
should avoid fetal morbidity and mortality in Acute events
like cord prolapse, severe abruption or scar rupture.
Prophylaxis and prediction
124

2/29/20
ELBOHOTY63
Standards for Intermittent Auscultation
• It is important that women are correctly identified
as low risk category for labor.
• Risk factor can change at any point during labor
necessitating a move to continuous EFM
125
Perinatal outcomes
50% reduction in neonatal seizures (RR0.50, 95%CI 0.31-0.80)
… but no significant difference in incidence of:
- long-term neurological handicap (RR1.74, 95%CI 0.97-3.11)
- or perinatal mortality (RR0.85, 95%CI 0.59-1.23)
Obstetric outcomes
- 66% increase in C. Section rate (RR1.66, 95%CI 1.30-2.13)
- 16% increase in instrumental delivery (RR1.16, 95%CI 1.01-1.32)
EFM vs. IA
126

2/29/20
ELBOHOTY64
127
Standards for Intermittent Auscultation
• For low-risk pregnancies, intermittent auscultation
should be offered and recommended in labor using
either a Doppler ultrasound, or a Pinard
stethoscope, to monitor fetal well-being.
128

2/29/20
ELBOHOTY65
1.Carry out intermittent auscultation immediately after a
contraction for at least 1 minute, at least every 15 minutes,
and record it as a single rate.
2.Record accelerations and decelerations if heard.
3.Palpate the maternal pulse hourly, or more often if there
are any concerns, to differentiate between the maternal
and fetal heartbeats.
129
Recommended regimen:
First stage of labor: at least every 15 minutes, after a contraction,
and for a minimum of 60 seconds.
Second stage of labor: every 5 minutes, after a contraction, and for
a minimum of 60 seconds.
Listening before or during a contraction does not detect late
decelerations.
130

2/29/20
ELBOHOTY66
Intermittent auscultation
• IA of the fetal heart rate should be offered to low-
risk women in established labour in all birth settings
• Potential problems:
• Standards are often not achievable on busy delivery suites
• Gradual changes, such as an increasing baseline, falling
variability or decelerations occurring during a contraction can
be missed
• There is no certification process for practitioners using
intermittent monitoring
• No hard record from the monitoring is generated and therefore
it is difficult to audit any guidelines related to performing the
technique
131
If there is a rising baseline fetal heart rate
or decelerations are suspected on
intermittent auscultation, actions should
include:
• carrying out intermittent auscultation more
frequently, for example after 3 consecutive
contractions initially
• thinking about the whole clinical picture, including
the woman's position and hydration, the strength
and frequency of contractions and maternal
observations.
132

2/29/20
ELBOHOTY67
If a rising baseline or decelerations are
confirmed, further actions should include:
• summoning help
• advising continuous cardiotocography, and
explaining to the woman and her birth
companion(s) why it is needed
• transferring the woman to obstetric-led care,
provided that it is safe and appropriate to do so
133
admission CTG
• The current evidence DOES NOT support the use of
the admission CTG in low-risk pregnancies
134

2/29/20
ELBOHOTY68
EFM
135
Evidence and NICE
• NICE advocate the use of continuous EFM in high-risk
labours.
• EFM use in high-risk labours improves outcomes
compared to low-risk labours.
• Randomised controlled trials comparing EFM and IA in
high-risk patients were performed in the 1970s and
early 80s but the number of participants was small
(<1000).
• Randomised control trials comparing EFM and IA in
high-risk patients in the present day might be argued to
be unethical to perform and, hence, NICE guidance is
based on observational studies.2/29/20 ELBOHOTY 136
136

2/29/20
ELBOHOTY69
There are a number of drawbacks and
limitations imposed by the use of EFM:
• Mobility
• Care in labour
• Analgesia in labour
• Increased intervention
• Variation in interpretation of CTG trace
• Litigation
137
Mobility
• Maternal mobility is inevitably reduced by being
attached to an electronic fetal monitor throughout
labour using the 'conventional' set-up.
• This may affect the progress of the labour and need
of analgesia
• NICE advises offering telemetry to any woman who
needs continuous cardiotography during labour.
• These EFM systems use radio waves and are
wireless. Women can remain mobile while being
monitored.
138

2/29/20
ELBOHOTY70
Care in labour
• In theory, attention may also switch from the
mother to the machine.
• Whatever kind of monitoring is being used, it is
important to keep the woman at the centre of care.
139
Analgesia in labour
• Both immobility and lack of support in labour may
affect the woman's ability to control and cope with
labour .
• Most EFM US transducers cannot be used in water,
which removes women's choice for this as an
analgesic.
• Newer telemetry transducers can be used in water,
allowing the woman to labour with greater mobility
and freedom.
140

2/29/20
ELBOHOTY71
Increased intervention
• Continuous EFM is associated with a significant
increase in caesarean section and instrumental
vaginal deliveries without an associated long-term
neonatal benefit .
• The incidence of caesarean section was lessened
when FBS was available
141
Variation in interpretation of CTG trace
• Inter-observer variation in the interpretation of an
abnormal CTG and recommendations for
intervention is a recognised problem.
• To improve reliability, uniform classification and
standardised training in CTG interpretation is
required. Hence this training package!
142

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ELBOHOTY72
Litigation
• The potential medico-legal problems from the use
of EFM
• Good record-keeping is crucial, whatever style of
monitoring is used.
•
143
Clinical Significance of Intrapartum CTG
• It is important to remember that the intrapartum
CTG is featured by having a high sensitivity, but
relatively low specificity. This means that:
– When the intrapartum CTG is normal, we can be fairly
confident that the fetus will be normoxic.
– When the intrapartum CTG is abnormal only 50% of
fetuses will show some degree of hypoxia.
– the predictive value of continuous EFM is improved by
the use of fetal blood sampling for pH.2/29/20 ELBOHOTY 144
144

2/29/20
ELBOHOTY73
Indications for continuous EFM
145
Advise continuous cardiotocography if any of the following risk factors
are present at initial assessment or arise during labour:
• maternal pulse over 120 beats/minute on 2 occasions 30 minutes apart
• temperature of 38°C or above on a single reading, or 37.5°C or above on 2
consecutive occasions 1 hour apart
• suspected chorioamnionitis or sepsis
• pain reported by the woman that differs from the pain normally associated with
contractions
• the presence of significant meconium
• fresh vaginal bleeding that develops in labour
• severe hypertension: a single reading of either systolic blood pressure of 160
mmHg or more or diastolic blood pressure of 110 mmHg or more, measured
between contractions
• hypertension: either systolic blood pressure of 140 mmHg or more or diastolic
blood pressure of 90 mmHg or more on 2 consecutive readings taken 30 minutes
apart, measured between contractions
• a reading of 2+ of protein on urinalysis and a single reading of either raised systolic
blood pressure (140 mmHg or more) or raised diastolic blood pressure (90 mmHg
or more)
• confirmed delay in the first or second stage of labour
• contractions that last longer than 60 seconds (hypertonus), or more than 5
contractions in 10 minutes (tachysystole)
• oxytocin use2/29/20 ELBOHOTY 146
146

2/29/20
ELBOHOTY74
• explain to the woman that it will restrict her mobility,
particularly if conventional monitoring is used
• encourage and help the woman to be as mobile as possible
and to change position as often as she wishes
•ensure that the focus of care remains on the woman rather
than the cardiotocograph trace
• ensure that the cardiotocograph trace is of high quality, and
think about other options if this is not the case
• bear in mind it is not possible to categorise or interpret
every cardiotocograph trace: senior obstetric input is
important in these cases.
If continuous cardiotocography is needed:
147
Overall care
• Make a documented systematic assessment of the condition of the
woman and unborn baby (including cardiotocography [CTG] ndings)
every hour, or more frequently if there are concerns.
• Do not make any decision about a woman's care in labour on the
basis of CTG ndings alone.
• Take into account the woman's preferences, any antenatal and
intrapartum risk factors, the current wellbeing of the woman and
unborn baby and the progress of labour.
• Ensure that the focus of care remains on the woman rather than the
CTG trace. Remain with the woman in order to continue providing
one-to-one support.
• Talk to the woman and her birth companion(s) about what is
happening and take her preferences into account.
148

2/29/20
ELBOHOTY75
Principles for intrapartum CTG trace
interpretation
• When reviewing the CTG trace, assess and document
contractions and all 4 features of fetal heart rate:
baseline rate; baseline variability; presence or absence
of decelerations (and concerning characteristics of
variable decelerations if present); presence of
accelerations.
• If there is a stable baseline fetal heart rate between 110
and 160 beats/minute and normal variability, continue
usual care as the risk of fetal acidosis is low.
• If it is difficult to categorise or interpret a CTG trace,
obtain a review by a senior midwife or a senior
obstetrician.
149
What would you do if a CTG recording was of
inadequate quality?
• Check transducer contact and all connections
• Check the maternal pulse again, and ensure you are
not recording this in error
• Consider use of ultrasound to detect and locate the
fetal heart and confirm its rate
• Consider use of a fetal scalp electrode if not
currently being used
150

2/29/20
ELBOHOTY76
Registration
It is necessary to record certain information on the CTG, to aid in both
identification and interpretation
• Name and registration number of the mother.
• Date and time of any recording.
• Maternal pulse rate at the beginning of the CTG.
• Posture of the mother and changes that occur.
• Speed of the paper.
• All drugs administrated to the mother.
• Cervical assessment and state of membranes and liquor
observed.
• Blood pressure recording before and after epidural
analgesia.
151
Interpretation of the
Intrapartum EFM
152

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ELBOHOTY77
Technical Considerations
• Maternal pulse should be palpated regularly with
any form of fetal monitoring, to differentiate
maternal and fetal heart rates:
– On rare occasions, it is possible to generate a signal from a large pulsating
maternal vessel.
153
154

2/29/20
ELBOHOTY78
Technical Standards for EFM
Paper Speed
155
1 cm/min
2 cm/min
3 cm/min
Paper
speed
156

2/29/20
ELBOHOTY79
157
Contraction Pattern
• Always remember to look at the “bottom line”. Take
notice of the duration of contractions and interval
between contractions.
158

2/29/20
ELBOHOTY80
159
160

2/29/20
ELBOHOTY81
161
162

2/29/20
ELBOHOTY82
163
What is the contraction frequency in
this CTG?
164

2/29/20
ELBOHOTY83
Contractions
• The optimum rate of contractions should not exceed
5:10.
• Tachysystole refers to > 5 contractions per 10-minute
period in 2 successive 10 minutes or averaged over 30
minutes.
• Hypertonus refers to excessive uterine contractions
lasting > 60 seconds.
• Hyperstimulation can be defined either as tachysystole,
that is, more than five contractions in 10 minutes over
a period of at least 20 minutes, or hypertonus, that is, a
contraction lasting for more than 2 mintues in
association with changes in the fetal heart trace.
• It occurs in 1–5% of prostaglandin-induced labour.
165
Tachysystole
> 5 contractions in 10 min in two successive 10-
min
periods, or averaged over 30 min.
166

2/29/20
ELBOHOTY84
Excessive contractions Fetal distress No
Sponteneous Refer for senior opinion.
Consider terbutaline
CEFM with close observation
Dinoprostone Tablet or gel Remove and wash for gel
Transfer to delivery suite.
If bishops score <8 or <3cms
leave
CEFM with close observation
Propess Remove propess. Transfer to
delivery suite with CEFM.
If bishops score <8 or <3cms
leave propess insitu . CEFM
with close observation
Oxytocin infusion Reduce by half current dose, a
response should be seen
within 5-10 minutes. If no
improvement stop infusion. In
cases of prolonged
deceleration (>3 mins) stop
Oxytocin immediately
Reduce Oxytocin to achieve
</= 5:10. Close observation for
signs of fetal distress
167
Management of Hyperstimulation
• Attempt removal of any remaining Dinoprostone gel
• Remove Dinoprostone pessary if still in situ
• Stop Oxytocin infusion while reassessing labour and fetal state
• Position woman left lateral
• Assess BP and FHR (EFM)
• Commence intravenous hydration if not contraindicated by maternal condition
• Pelvic exam to assess cervical dilation
• If persists use tocolytics:
– Salbutamol 125 μg at 25 μ/min IV. One 1 ml vial (0.5 mg/ml) in 100 ml of crystalloid
solution, in intravenous perfusion at 300 ml/h for 5 min
– Terbutaline 0.25 mg by subcutaneous injection
– Atosiban 6.75 mg IV. One 0.9 ml vial (7.5 mg/ml) given by intravenous bolus during 1
min
• Prolonged decelerations should start to revert 1–2 min after acute tocolysis has
begun, and waiting for this to occur is the first option when hypercontractility is
strongly suspected.
• During the second stage of labour, instrumental vaginal delivery may be an
alternative if there are conditions for a quick and safe procedure
• If clinically indicated perform emergency CS
168

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ELBOHOTY85
Frequent, low amplitude contractions, in
association with abnormal CTG, is suggestive
of placental abruption.
169
1. presence of accelerations.
2. baseline fetal heart rate
3. baseline variability
4. presence or absence of decelerations
When reviewing the CTG trace, assess and
document all 4 features
170

2/29/20
ELBOHOTY86
171
Abrupt increases in FHR above baseline, > 15 bpm
amplitude, > 15 secs
Accelerations
• Most coincide with fetal movements
• Reactive fetus without hypoxia/acidosis
150
130
140
120
>15 s
>15 bpm
172

2/29/20
ELBOHOTY87
Significance
• Fetal heart rate increases due to activity in utero which
is controlled through the somatic nervous system, it is
recorded on the CTG as an acceleration. These
accelerations are considered as hallmarks of fetal
wellbeing
• If repeated accelerations are present with reduced
variability, the CTG should be regarded as normal
• Remember, the absence of accelerations with an
otherwise normal CTG is of uncertain significance,
however a sick or hypoxic fetus exposed to significant
intrapartum hypoxia would reduce its movements and
therefore is unlikely to show accelerations.
• Continue to risk assess and review the clinical picture
as a whole when making your interpretation
173
• <32 weeks' : >10 BPM above baseline for >10 seconds
• >32 weeks' : >15 BPM above baseline for > 15 seconds.
Accelerations
174

2/29/20
ELBOHOTY88
•The presence of fetal heart rate accelerations is
generally a sign that the unborn baby is healthy.
•If a fetal blood sample is indicated and the
sample cannot be obtained, but the associated
scalp stimulation results in fetal heart rate
accelerations, decide whether to continue the
labour or expedite the birth in light of the
clinical circumstances and in discussion with the
woman.
175
176

2/29/20
ELBOHOTY89
Acceleration
177
Misinterpretation
• Be suspicious of CTG’s where accelerations exactly
mirror contractions – are you picking up maternal
pulse?
• In this situation FH must be confirmed with sonicaid
or USS and the transducer repositioned FSE
applied.
178

2/29/20
ELBOHOTY90
BASELINE RATE
Mean level of the most horizontal and less oscillatory FHR
segments. Estimated in 10-min periods, expressed in bpm
Intrapartum CTG Reassuring Non-Reassuring Abnormal
Baseline rate 110 – 160 bpm 100-109 bpm
161 – 180 bpm
< 100 bpm
> 180 bpm
Although a baseline fetal heart rate between 100 and 109 beats/minute is a non-reassuring
feature, continue usual care if there is normal baseline variability and no variable or late
decelerations.
179
180

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ELBOHOTY91
Uncomplicated Tachycardia
• A tachycardic baseline is 161-180 bpm.
• An uncomplicated tachycardia (where no other
abnormal features appear) should be regarded as non-
reassuring but may be caused by
– a period of fetal activity which then settles
– a maternal pyrexia (treat maternal pyrexia, IV fluids,
Paracetamol)
– maternal tachycardia (take steps to correct, IV fluids, temp
check)
– the administration of certain drugs (MgSo4, hydralazine)
– changes in placental blood flow (change maternal position).
– Gestation <32 weeks
• Record any events on the CTG2/29/20 ELBOHOTY 181
181
Complicated Tachycardia
• Gradually evolving tachycardia describes an
increase in baseline rate, even within the normal
range, but with other non-reassuring or abnormal
features present, should increase concern of
hypoxia
• Significant Fetal Tachycardia (FHR >180 bpm)
• Fetal arrhythmia or congenital defect (FHR >200
bpm)
• Fetal infection
182

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ELBOHOTY92
If the baseline fetal heart rate is above 180 beats/minute with no
other non-reassuring or abnormal features on the cardiotocography
• Think about possible underlying causes (such
as infection) and appropriate investigation.
• check the woman's temperature and pulse; if
either are raised, offer fluids and paracetamol
183
• Fetal bradycardia is commonly associated with fetal
hypoxemia. However, a number of causes must be
considered;
– Drugs eg.benzodiazepines, beta blockers
– maternal hypotension
– Hypothermia
– maternal hypoglycaemia,
– fetal brady arrhythmias
– complete heart block
– congenital heart block
– umbilical cord compression
– amniotic fluid embolism
– normal variation
• An FSE can be useful with a bradycardic baseline to exclude
the possibility of mistakenly recording maternal pulse rate2/29/20 ELBOHOTY 184
184

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ELBOHOTY93
Normal Baseline FHR
185
186

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ELBOHOTY94
Baseline Tachycardia
187
This is the difference between the upper and lower limits of the
baseline heart rate (Average bandwidth amplitude)
over one minute
188

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ELBOHOTY95
Variability
189
Baseline Variability
• Normal variability greater than 5bpm
• Baseline variability is the degree to which the baseline
varies within a band width excluding any accelerations
or decelerations
• Normal baseline variably shows good autonomic
control with alternating cycles of reduced and
increased variability
• Fetus that are neurologically stable have quiet/sleep
periods and active periods.
• It should be assessed during a reactive 1 minute period
• This is known as cycling, absence of cycling can be an
indication of hypoxia.
190

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ELBOHOTY96
Reasons for reduced variability include
• sleep phase
– intermittent periods of reduced baseline variability are
normal, especially during periods of quiescence ('sleep')
• Prematurity
• fetal tachycardia
• Drugs
• congenital malformation
• cardiac arrhythmias
• fetal anaemia
• fetal infection
191
What is your comment
Normal cycling
192

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ELBOHOTY97
FHR Variability
Absent variability =
Amplitude range undetectable
Minimal = < 5 BPM
Moderate = 6 to 25 BPM
Marked = > 25 BPM
Saltatory pattren:The pathophysiology of this pattern is incompletely understood. It is presumed to be
caused by fetal autonomic instability/hyperactive autonomic system . You cannt determine the baseline
heart rate
193
Variability
Variability 5 bpm or more Less than 5 for 30 to 50 minutes
OR
More than 25 for 15 to 25
minutes
Less than 5 for more than
50 minutes
OR
More than 25 for more than
25 minutes
OR Sinusoidal
194

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ELBOHOTY98
Reduced Variability
195
Reduced Variability
196

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ELBOHOTY99
Saltatory rhythm
197
Increased
variability
(saltatory)
Bandwidth > 25 bpm for more than 25 min
• Incompletely understood
• Hypoxia/acidosis of rapid evolution
198

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ELBOHOTY100
Sinusoidal patterns
• A regular oscillation of the baseline long-term
variability (resembling a sine wave).
• Smooth, undulating pattern, lasting at least 10
minutes, has a relatively fixed period of 3-5 cycles
per minute at an amplitude of 5-15 beats per
minute above and below the baseline.
199
• Severe anemia, haemoglobinopathies, feto-maternal hemorrhage or
bleeding from the fetus (abruption/vasa praevia) or hypoxia acute
hypoxia/acidosis, infection, cardiac malformations, hydrocephalus,
gastroschisis,
Sinusoidal
pattern
Regular, smooth, undulating, resembling
sine wave. Amplitude 5-15 bpm, frequency
3-5 cycles/min, > 30 min, no accelerations
The incidence of true sinusoidal FHR pattern is rare, reportedly between 0.3 to 1.7%.
Most importantly there will be NO areas of normal FHR variability and NO accelerations.
True sinusoidal FHR pattern is an ominous FHR pattern needing immediate fetal evaluation and
possible intervention based on individual case details and gestational age especialy if it was
found in non labouring woman
200

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ELBOHOTY101
sinusoidal pattern
201
202

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ELBOHOTY102
It is important to realise that not all severely anaemic fetus show a
sinusoidal pattern.
A normal CTG with intermittent areas of sinusoidal pattern suggests that
the fetus is sucking its thumb, a change in position of the mother should
rectify this if concerned.
203
Pseudo-sinusoidal pattern
• Mild or minor pseudo-sinusoidal patterns (oscillations of amplitude 5–15 beats/minute) are of no
significance.
• Analgesic administration, fetal sucking and other mouth movements
Pseudo-
sinusoidal
pattern
Jagged “saw-tooth” appearance. Duration
seldom exceeds 30 min. Normal patterns
before and after
204

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ELBOHOTY103
Psedosinusoidal Pattern
205
Pseudosinusoidal pattern
• A pattern resembling the sinusoidal pattern, but
with a more jagged “saw-tooth” appearance, rather
than the smooth sine-wave form.
• Its duration seldom exceeds 30 minutes and it is
characterized by normal patterns before and after.
• This pattern has been described after analgesic
administration to the mother, and during periods of
fetal sucking and other mouth movements.
• It is sometimes difficult to distinguish the
pseudosinusoidal pattern from the true sinusoidal
pattern, leaving the short duration of the former as
the most important variable to discriminate
between the two.2/29/20 ELBOHOTY 206
206

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ELBOHOTY104
Decelerations
• Decelerations are defined as a drop in heart rate of
more than 15 beats, lasting for more than 15
seconds.
• Decelerations may be significant as they may be
related to developing hypoxia
• The majority of decelerations have NO relation to
hypoxia but are caused by mechanical changes in
the fetal environment i.e. head and cord being
compressed
207
Decelerations
When describing decelerations in fetal heart,
• rate the depth and duration of the individual
decelerations.
• Their timing in relation to the peaks of the
contractions
• Whether or not the fetal heart rate returns to
baseline
• How long they have been present for
• Whether they occur with over 50% of contractions.
208

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ELBOHOTY105
When describing decelerations in fetal
heart rate, specify:
• their timing in relation to the peaks of the
contractions the duration of the individual
decelerations
• whether or not the fetal heart rate returns to
baseline
• how long they have been present for
• whether they occur with over 50% of contractions
• the presence or absence of a biphasic (W) shape
• the presence or absence of shouldering
• the presence or absence of reduced variability
within the deceleration2/29/20 ELBOHOTY 209
209
There are 5 types of decelerations:
– Early deceleration
– Late deceleration
– Variable deceleration
– Prolonged deceleration
– Shallow deceleration with low variability
210

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ELBOHOTY106
Describe decelerations as ‘early’, ‘variable’ or ‘late’.
Do not use the terms ‘typical’ and ‘atypical’ because they
can cause confusion (NICE!)2/29/20 ELBOHOTY 211
211
• From 26 weeks onwards decelerations of the
fetal heart should be regarded as abnormal.
However, fetal decelerations are a normal
feature before 26 weeks
212

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ELBOHOTY107
213
Early Decelerations
• Uniform, repetitive, periodic slowing of the FHR with
onset early in the contraction and return to baseline at
the end of contraction.
• Early decelerations are considered as normal, they are
caused by head compression so are more common in
the latter 1st stage and 2nd stage of labour.
• They mirror the contraction peaks exactly, are
associated with compression and rarely fetal hypoxia
(The lowest point of the deceleration coincides with the
highest point of the contraction wave).
• Early decelerations with no non-reassuring or abnormal
features on the cardiotocograph trace should not
prompt further action.
214

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ELBOHOTY108
Early Decelerations
215
Early Decelerations
216

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ELBOHOTY109
Late Decelerations
• Uniform, repetitive, periodic slowing of the FHR with
onset mid- to the end of the contraction.
• There is a time lag between the onset and peak of the
contraction and the onset and peak of the deceleration.
• They are frequently associated with an increase in
baseline heart rate
• They may also be linked to short lasting hypoxia,
related to a reduction in placental blood flow. They are
often associated with abnormal uterine activity and
may be seen in relation to placental insufficiency and
are more commonly seen in cases such as abruption,
hyperstimulation, aortocaval compression.
• Late decelerations, if present for > 30 minutes, are
indicative of fetal hypoxia, and further actions is
indicated.2/29/20 ELBOHOTY 217
217
Mechanism
• There is oxygenated blood in the retro placental
space.
• As a contraction starts the fetus uses up this
reservoir.
• Due to a restricted blood supply a hypoxic
deceleration happens and will only recover
sometime after a contraction when fully
oxygenated blood has been restored
218

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ELBOHOTY110
219
Late Decelerations
220

2/29/20
ELBOHOTY111
221
Late Decelerations
222

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ELBOHOTY112
Late Decelerations
223
Variable Decelerations
• The MOST COMMON form of decelerations
occurring during labor.
• Variable decelerations are often caused by umbilical
cord compression.
• It can be:
– Uncomplicated
– Complicated
224

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ELBOHOTY113
Uncomplicated Variable Decelerations
• They are the most common type of decelerations
and are called ‘variable’ because they vary in shape,
size and sometimes in timing with respect to each
other.
• Less than 60 beat drop for less than 60 seconds =
uncomplicated
• Usually rapid descent and rapid recovery.
• They vary because they are a manifestation of
umbilical cord compression and it is compressed in
a slightly different way each time.
• They are more often seen with reduced amniotic
fluid volume
225
Mechanism
• Initial or mild umbilical cord compression results in occlusion of the
umbilical vein, which is larger than the arteries and less rigid. This
results in decreased venous return resulting in reflex tachycardia to
maintain cardiac output.
• This explains the often seen initial increase in heart rate (shoulder)
preceding the deceleration.
• Further compression of the cord leads to occlusion of the umbilical
artery, and the resulting increased systemic resistance, sensed by the
baroreceptors, results in a protective reflex slowing of the heart rate.
As the cord is decompressed, this series of events is reversed, and a
‘shoulder’ may follow the deceleration (artery is decompressed but
the vein is still compressed) prior to returning to baseline
• A normal, well grown fetus can tolerate cord compression for a
considerable length of time before becoming hypoxic.
226

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ELBOHOTY114
227
228

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ELBOHOTY115
229
concerning Variable Decelerations
• lasting more than 60 seconds
• reduced baseline variability within the deceleration
• failure to return to baseline
• biphasic (W) shape
• no shouldering.
230

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ELBOHOTY116
231
232

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ELBOHOTY117
Variable deceleration dropping from
baseline by >60 bpm or taking >60 seconds
to recover
233
Prolonged Deceleration/Bradycardia
• Single deceleration lasting over 3 minutes is termed
prolonged decelerations, lasting over 10 minutes, is
a baseline change; bradycardia.
• 90% of prolonged deceleration without incidences
(rupture, abruption, cord prolapse,
hyperstimulation) will return to baseline within 6
minutes and 95% within 9 minutes.
• Summon help and prepare the patient for
theatre...you don’t have to go!
234

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ELBOHOTY118
235
236

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ELBOHOTY119
Prolonged Decelerations
237
Management
• Clinicians should exclude three major accidents during labour
– Abruption
– cord prolapse
– caesarean scar rupture
• If there is any clinical evidence of these accidents, an immediate
delivery should be undertaken to salvage the fetus.
• This is because metabolic acidosis is likely to get worse with time
due to continued reduction in the utero-placental circulation.
• Other reversible causes of acute bradycardia
• epidural top up
• vaginal examination
• uterine hyperstimulation.
• In more than 50% of cases, no cause may be identified.
• In cases of uterine hyperstimulation, oxytocin infusion should be
stopped immediately and tocolytics (terbulatine 250 mcg
subcutaneously) administered, if required, to abolish the uterine
contraction.
238

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ELBOHOTY120
• If the three accidents are excluded, it is reasonable to
wait, particularly if the variability of the heart rate
during the episode of deceleration or bradycardia is
normal and if the CTG prior to the deceleration was
normal.
• Reduced variability prior to the onset of bradycardia
has been reported to be associated with a poor
outcome.
• It is estimated that in the absence of the three
accidents of labour, over 90% of CTGs with prolonged
bradycardia are likely to recover to normal baseline in
six minutes and up to 95% in nine minutes.
• Signs of recovery to the normal baseline (i.e. an upward
trend of the end of the deceleration, repeated attempts
to reach the baseline) are also a positive feature.
239
Guidance on the management of
prolonged decelerations
• This guidance (referred to as the '3,6,9,12 and 15 minute
guidance') involves instituting appropriate interventions
• At 3 minutes start:
– Positioning
– Hydration
– Tocolysis
– stopping syntocinon infusion
• At 6 minutes:
– move the patient to theatre by nine minutes if the CTG shows no
recovery.
• At 9 minutes:
– Prepare to deliver
• At 12 minutes:
– attempts at delivery should commence by At 15 minutes:
Delivery122/29/20 ELBOHOTY 240
240

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ELBOHOTY121
cases of sudden maternal cardiorespiratory arrest.
• the interval between arrest and birth was under 12
min: No long-term neurological sequelae were
reported when
• the interval between arrest and birth was more
than 15 min: perinatal death
• This is only valid for normally grown fetuses at
term, receiving adequate oxygenation before the
insult occurred, and needs to be adapted in other
situations.
241
242

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ELBOHOTY122
243
Decelerations None or early
Variable
decelerations
with no
concerning
characteristics
* for less than
90 minutes
Variable decelerations:
•with no concerning characteristics
for 90 minutes or more
•OR
•with any concerning
characteristics in up to 50% of
contractions for 30 minutes or
more
•OR
• with any concerning
characteristics in over 50% of
contractions for less than 30
minutes
Late decelerations:
in over 50% of contractions for less
than 30 minutes, with no maternal
or fetal clinical risk factors such as
vaginal bleeding or signi cant
meconium
with any concerning
characteristics in over 50%
of contractions for
30 minutes (or less if any
maternal or fetal clinical
risk factors
Late decelerations:
for 30 minutes (or less if
any maternal or fetal
clinical risk factors)
Bradycardia / single
prolonged deceleration >3
mins
244

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ELBOHOTY123
How to read a CTG?
Overall :Comments & management
Dr C BRAVADO
When a CTG is reviewed you should always
look at the clincial picture. Beware of
MOTHERS:
Meconium
Oxytocin
Temperature
Hyperstimulation/haemorrhage
Epidural
Rate of progress
Scar.
245
Baseline rate 110 – 160 bpm
100-110 with
normal
variability
100-109 bpm
161 – 180 bpm
< 100 bpm
> 180 bpm
Variability 5 bpm or more Less than 5 for 30 to 50 minutes
OR
More than 25 for 15 to 25 minutes
Less than 5 for more than
50 minutes
OR
More than 25 for more than
25 minutes
OR Sinusoidal
Decelerations None or early
Variable
decelerations
with no
concerning
characteristics
for less than 90
minutes
•with no concerning characteristics for 90
minutes or more
•OR
•with any concerning characteristics in up
to 50% of contractions for 30 minutes or
more
•OR
• with any concerning characteristics in
over 50% of contractions for less than 30
minutes
Late decelerations:
in over 50% of contractions for less than
30 minutes, with no maternal or fetal
clinical risk factors such as vaginal
bleeding or significant meconium
with any concerning characteristics
in over 50% of contractions for
30 minutes (or less if any maternal
or fetal clinical risk factors
Late decelerations:
for 30 minutes (or less if any
maternal or fetal clinical risk factors)
Bradycardia / single prolonged
deceleration >3 mins
246

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ELBOHOTY124
Urgent birth
Bradycardia or a
single prolonged
deceleration with
baseline below
100 beats/minute,
persisting for
3 minutes or more
PATHOLOGICAL
1 abnormal feature
OR
2 non-reassuring
features
SUSPECIOUS
1 non-reassuring
feature
AND
2 normal/
reassuring
features
NORMAL
All 3 features are
normal/ reassuring
1. Urgently seek obstetric help
2. If there has been an acute
event (for example, cord
prolapse, suspected placental
abruption or suspected
uterine rupture), expedite the
birth
3. Correct any underlying
causes, such as hypotension
or uterine hyperstimulation
4. Start 1 or more conservative
measures Make preparations
for an urgent birth
5. Expedite the birth if the acute
bradycardia persists for 9
minutes
6. If the fetal heart rate recovers
at any time up to 9 minutes,
reassess any decision to
expedite the birth, in
discussion with the woman
1. Obtain a review by an
obstetrician and a senior
midwife
2. Exclude acute events (for
example, cord prolapse,
suspected placental abruption
or suspected uterine rupture)
3. Correct any underlying causes,
such as hypotension or uterine
hyperstimulation
4. Start 1 or more conservative
measures
5. If the cardiotocograph trace is
still pathological after
implementing conservative
measures:
6. offer digital fetal scalp
stimulation
7. If the cardiotocograph trace is
still pathological after fetal
scalp stimulation:
8. consider fetal blood sampling
consider expediting the birth
take the woman's preferences
into account
1. Correct any underlying
causes, such as
hypotension or uterine
hyperstimulation
2. Perform a full set of
maternal observations
3. Start 1 or more
conservative measures*
4. Inform an obstetrician or a
senior midwife
5. Document a plan for
reviewing the whole
clinical picture and the
CTG ndings
6. Talk to the woman and her
birth companion(s) about
what is happening and
take her preferences into
account
1. Continue CTG and
normal care.
2. If CTG was started
because of concerns
arising from
intermittent
auscultation, remove
CTG after 20 minutes if
there are no non-
reassuring or abnormal
features and no ongoing
risk factors.
247
FIGO
248

2/29/20
ELBOHOTY125
FIGO CONSENSUS GUIDELINES ON
INTRAPARTUM FETAL MONITORING
Tracing classification
*Decelerations are repetitive when associated with > 80% contractions.
Absence of accelerations during labour is of uncertain significance.
Baseline
Variability
Decelerations
Interpretation
Clinical
Management
Normal
110-160 bpm
5-25 bpm
No repetitive*
decelerations
Suspicious
Lacking at least one
characteristic of
normality, but with
no pathological
features
Pathological
< 100 bpm
Reduced variability
Increased variability, or
sinusoidal pattern
Repetitive* late or prolonged
decelerations > 30 min or > 20 min
if variability is reduced.
Prolonged deceleration > 5 min
No
hypoxia/acidosis
No intervention
necessary
Low probability of
hypoxia/acidosis
Action to correct
reversible causes,
close monitoring, or
adjunct technologies
High probability of
hypoxia/acidosis
Immediate action to correct
reversible causes, adjunct
technologies or if not possible
expedite delivery.
In acute situations, immediate
delivery must be accomplished.
249
Conservative care
Ensure adequate quality recording of both FHR and contraction pattern
Inadequate quality CTG?
-Check maternal pulse.
- Poor contact from external transducer? check position
of transducer.
- Internal transducer
Uterine hypercontractility?
-Is the mother receiving oxytocin?
-Reduce/stop infusion.
- Has the mother recently received vaginal dinoprost?
- Consider tocolysis with subcutaneous terbutaline
0.25 mg.
Maternal tachycardia/pyrexia
-Is there maternal infection?
- check temperature. If 37.5°C on two occasions or
38.0°C or higher, consider screening and treatment.
-Is mother dehydrated?
- check blood pressure and give IV 500 ml crystalloid
if appropriate.
-Is mother receiving tocolytic infusion?
- if maternal pulse > 140 bpm, reduce infusion.
Other Maternal Factors
What is the mother’s position?
-Encourage mother to adopt left-lateral position.
Consider
-Is mother hypotensive?
-Has a vaginal examination just been performed?
- Has mother been vomiting or had a vasovagal
episode?
-Has mother just had epidural sited?
Check blood pressure and give IV 500 ml crystalloid if
appropriate
250

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ELBOHOTY126
Reversible hypoxia/acidosis
Tachyssystole
Iatrogenic/spontaneous excessive contraction frequency
Maternal supine position
(aorto-caval compression by pregnant uterus)
Sudden maternal hypotension
(following epidural or spinal analgesia)
Maternal respiratory complications
Acute asma, etc.
251
Intra-uterine resuscitation
• In a number of cases, various steps can be taken to
revert the CTG changes and alleviate the pathology
causing these changes. Some of these steps are
described in the following pages:
• Alteration of maternal position
• Hydration
• Reduction or abolition of uterine activity / acute
tocolysis
Do not use maternal facial oxygen therapy for intrauterine fetal resuscitation,
because it may harm the baby (but it can be used where it is administered for
maternal indications such as hypoxia or as part of preoxygenation before a
potential anaesthetic).
252

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ELBOHOTY127
Hydration
• In conditions where hypotension is expected (e.g.
epidural anaesthesia or analgesia and cases of
maternal bleeding), it is important to keep the
women well hydrated to prevent maternal
hypotension, reduction in utero–placental perfusion
and FHR changes.
253
Sudden maternal hypotension
• It is secondary to epidural or spinal analgesia is usually
quickly reversed by starting or increasing crystalloid
perfusion and when this is not enough administering
ephedrine 3–6 mg in intravenous bolus over 5 min.
• The bolus can be repeated after 5–10 min, until a
maximum dose of 10 mg is reached. The drug is
contraindicated in patients with cardiac disease,
hypertension, hyperthyroidism, phaeocromocytoma
and closed angle glaucoma and those who have taken
monoamine oxidase inhibitors in the previous 14 days.
• The following side effects have been reported:
paleness, fever, dry mucosae, shortness of breath,
chest pain, tachycardia, anxiety, nausea and vomiting,
headache, insomnia and mood changes.
• It can also cause transitory fetal tachycardia.2/29/20 ELBOHOTY 254
254

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ELBOHOTY128
Reduction or abolition of uterine activity /
acute tocolysis
• Inhibition of uterine activity is useful when there is
abnormal uterine activity
• In the presence of a grossly abnormal FHR, the fetal
blood pH can drop drastically within a very short period
of time in the presence of uterine contractions
• In these situations, and in cases where fetal distress is
related to uterine hyperactivity, inhibition of uterine
activity with a bolus intravenous dose of betamimetic
drugs such as terbutaline (0.25 mg in 5 ml of saline
slow iv or 0.25 mg/ml sc) or ritodrine (6 mg in 5 ml of
physiological saline iv) may be of value as a temporary
expedient.
255
Excessive uterine activity should be
avoided, irrespective of FHR changes,
reversed by ¯ ocytocin or acute tocolysis
• Salbutamol
• Terbutaline
• Ritodrine
• Atosiban
• Nitroglycerine
256

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ELBOHOTY129
Fetal scalp stimulation
257
Pathological CTG
CTG is still
pathological
fetal scalp stimulation
Failed
conservative
measures
Fetal blood sample
if appropriate otherwise urgent
delivery is considered
Acceleration
review the whole
clinical picture.
258

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ELBOHOTY130
Fetal blood sample
259
The idea behind FBS
• CTG is a screening test and carries a false +ve results
up to 50 %.
• So it is plausible to backup the abnormal results
with an a diagnostic test.
• Fetal scalp pH or lactate assessment is considered
an objective reliable test to diagnose intrapartum
hypoxia
260

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ELBOHOTY131
• in contrast with conditions causing acute hypoxic
insults, the hypoxic stress of labour may cause an
abnormal fetal heart rate (FHR) up to 90 minutes
prior to a fall in scalp pH. This is why it is important
to repeat fetal blood sampling if the FHR
abnormality persists.
• An increasing degree of CTG abnormality is
associated with a higher likelihood of low scalp pH
261
Fetal Blood Sampling
• It is an invasive procedure however it
helps to reduce the need for further,
more serious interventions .
• It should be advised in the presence
of an abnormal FHR trace, unless
there is clear evidence of acute
compromise.
262

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ELBOHOTY132
Fetal Scalp Blood Sampling prerequisites
• Maternal Consent
• Requires rupture of
membranes
• Cervix is dilated 4 cm
• No contraindication
263
Fetal blood sampling is inappropriate in:
1. Where there is clear evidence of acute fetal
compromise (e.g. Prolonged deceleration greater
than three minutes, cord prolapse, antepartum
haemorrhage,…..), fetal blood sampling should
not be undertaken and the baby should be
delivered urgently.
2. Maternal viral infection (e.g. hepatitis viruses and
herpes simplex virus)
3. Fetal bleeding disorders (e.g. Haemophilia)
4. Prematurity (< 34 weeks).
5. Face presentation
264

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ELBOHOTY133
Requirements
• Conical Speculum/Amnioscope and KY jelly
• Ethyl chloride
• Sponge-holder
• Cotton wool / 4 x 3cm swabs
• Petroleum jelly
• Heparinised capillary tube
• Blood gas machine
265
266

2/29/20
ELBOHOTY134
A special ready kit
267
Maternal Position
• The preferred maternal position is
left-lateral position with hips well
flexed and the lower leg extended.
268

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ELBOHOTY135
Steps
• Attach the fetal scalp blade (depth of 2 mm) to an
introducer
• Insert the amnioscope into the vagina, so that the narrow
end rests on the fetal scalp (away from any fontanelles).
• Clean any blood/mucous off the fetal scalp
• Spray with ethyl chloride.
• Dab with petroleum jelly (prevents the fetal blood from
flowing away)
• Make a small nick in the fetal scalp with the
needle/stylette.
• Collect the resulting blood in the heparinised capillary tube
• Insert into the blood gas machine in order to obtain the pH.
• Interpret results .
269
Video
270

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ELBOHOTY136
pH ≤7.2 7.21-7.23 ≥7.24
Lactate
(mmol/L)
≥4.9 4.2-4.8 ≤4.1
Interperitation Abnormal Borderline Normal
Action Delivery
indicated
e.g. Catergory 1
CS or OVD
Repeat after 30
minutes if CTG
remains the same
Repeat after 60
minutes if CTG
remains the
same
Interpretation
271
• Discuss with a consultant obstetrician if a third fetal blood sample is thought to be needed.
272

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ELBOHOTY137
When a fetal blood sample cannot be
obtained
• If fetal blood sampling is attempted and a sample
cannot be obtained, but the associated fetal scalp
stimulation results in a fetal heart rate acceleration,
decide whether to continue the labour or expedite
the birth in light of the clinical circumstances and in
discussion with the woman and a senior
obstetrician.
• If fetal blood sampling is attempted but a sample
cannot be obtained and there has been no
improvement in the cardiotocograph trace,
expedite the birth2/29/20 ELBOHOTY 273
273
Postnatal assesment
• Paired cord blood sample
• Apgar score
• Neonatal seizures
• Organ damage
• Cerebral palsy.
• Neurodevelopmental disability.
• Death
274

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ELBOHOTY138
275
Blood gas or lactate analysis
• in the umbilical cord, or in the newborn circulation during the first minutes of life,
is the only objective way of quantifying hypoxia/acidosis occurring just prior to birth
276

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ELBOHOTY139
Cord blood sampling
• Unnecessary to clamp the cord
• As soon as possible after birth (< 15 min)
• Artery and vein
• Analysis within 30 min
277
Paired cord samples
• Paired cord samples should not be taken
routinely on all births
• Paired cord samples should be taken on all births
in which there has been concern regarding fetal
wellbeing or admission to neonatal unit is
expected
278

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ELBOHOTY140
Those are normal umbilical vein and
artery blood gases.
Venous Arterial
pH 7.35 (± 0.05) 7.28 (± 0.05)
PCO2 38 (± 5.6) 49 (± 8.4)
PO2 29 (± 5.9) 18 (± 6.2)
BE* -4 (± 2) -4 (± 2)
279
280

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ELBOHOTY141
281
282

2/29/20
ELBOHOTY142
CO2 increases early
So it is called
Respirator y Acidosis
After
consumption
of HCO3 , pH
shows more
drop with
resultant
Metabolic or
Mixed Acidosis
283
Respiratory acidosis
• Acidemia in the artery only and BE > -10
284

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ELBOHOTY143
CHRONIC FETAL DISTRESS
(METABOLIC OR MIXED):
CO2 can diffuse rapidly across the
placenta, H+ and lactate take much
longer to equilibrate. So acidaemia
occurs in both artery and vein.
285
Metabolic acidosis
Arterial pH < 7.00 and BD >12 mmol/l
Arterial lactate > 10 mmol/l is an alternative,
but reference values may vary according to
device
286

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ELBOHOTY144
Apgar score
• The most widely used indicator of fetal condition at
birth is the Apgar score
• The Apgar score is designed to give an overview of
the fetal condition at set times following birth and
identify those babies in need of resuscitation.
• Low Apgar scores are not synonymous with hypoxia,
acidosis or asphyxia
• There are various causes of poor Apgar scores at
birth.
287
2882/29/20 ELBOHOTY
288

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ELBOHOTY145
1-minute Apgar
• important to decide newborn resuscitation
• low association with intrapartum
hypoxia/acidosis
5-minute Apgar
• stronger association with short- and long-term
neurological outcome and neonatal death
289
Unaffected by minor degrees of hypoxia/acidosis
Subject to interobserver disagreement
Affected by non-hypoxic causes::
• prematurity
• birth trauma
• infection
• meconium aspiration
• congenital anomalies
• pre-existing neurological lesions
• medication administered to the mother
• early endotracheal aspiration
Apgar scores
290

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ELBOHOTY146
Metabolic acidosis and low Apgars
• vast majority recover quickly and have no short- or
long-term complications
• few cases are of sufficient intensity and duration to
cause death or long-term morbidity
291
Hypoxic-ischemic encephalopathy (HIE)
• Short-term neurological dysfunction caused by
hypoxia/acidosis
• Metabolic acidosis, low Apgars, early imaging of
cerebral edema, changes in muscle tone, sucking
difficulties, seizures or coma in first 48 h of life
• May be accompanied by other system dysfunctions
292

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ELBOHOTY147
• other non-hypoxic causes
• need to document metabolic acidosis in
umbilical artery or in newborn circulation
during the first minutes of life for HIE
Neonatal encephalopathy
293
Infection
Congenital diseases
Metabolic diseases
Coagulation disorders
Antepartum and post-natal hypoxia
Birth trauma
• Manifests at 1-4 years
• Long-term neurological complication more commonly
associated with term intrapartum hypoxia/acidosis
• Only 10-20% cases are caused by hypoxia/acidosis
Cerebral palsy (spastic quadriplegic , dyskinetic )
294

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ELBOHOTY148
• Metabolic acidosis
• Low 1 and 5-minute Apgar scores
• Grade 2 or 3 HIE
• Early imaging of acute non-focal cerebral anomaly
• Spastic quadriplegic or dyskinetic type
• Exclude other identifiable etiologies
Intrapartum hypoxia/acidosis as the cause of
cerebal palsy in term infants
295
Outcome Measures of Perinatal
Ischemia/Hypoxia
Intermediate Outcome Measures
• Umbilical artery acidemia at birth correlates with
neonatal complications.
• A five-minute Apgar score equal to or less than three
may be a sensitive marker of long-term sequelae.
• The development of moderate or severe neonatal
encephalopathy appears to be the most robust
intermediate outcome measure of potential long-term
disability.2/29/20 ELBOHOTY 296
296

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ELBOHOTY149
Outcome Measures of Perinatal
Ischemia/Hypoxia
Outcomes of Poor Association
• Apgar scores at one minute are not a robust marker.
• Neonatal convulsions alone are a poor marker of
intrapartum hypoxic injury.
• The need for either neonatal resuscitation/ ventilation
or admission to neonatal intensive care units in
isolation are not predictive of long-term neurological
sequelae.2/29/20 ELBOHOTY 297
297
Progressively increasing degrees of hypoxic injury to the fetus in labour
can result in damage to the central nervous system which eventually
can become irreversible.
The syndrome that is manifest in the newborn is HIE. There are three
grades of severity.
The likelihood of death or severe disability is greater the higher the HIE
grades.
Levene ML, Kornberg J, Williams TH. The incidence and severity of post-
asphyxial encephalopathy in full-term infants. Early Hum Dev 1985;11:21-26
Hypoxic ischemic encephalpoathy
298

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ELBOHOTY150
299
300

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ELBOHOTY151
Cerebral palsy
• Cerebral palsy is a group of permanent disorders of the development of movement
and posture, causing activity limitation, that are attributed to non-progressive
disturbances that occurred in the developing fetal or infant brain.
• In the context of this session we are concerned with those cases that are caused
by IP hypoxia.
• Five categories are recognized:
• Hemiplegia
• Spastic quadriplegia
• Diplegia
• Ataxia
• Dyskinesis
• The commonest features of hypoxic injury are spasticity affecting all four limbs and
hypotonia
301
Cerebral palsy
There are seven criteria that should ideally be met for a case of cerebral palsy
to be causally linked to acute intrapartum hypoxia. The two most specific are:
• 1. Evidence of metabolic acidosis in intrapartum umbilical cord at arterial
or very early neonatal sample(pH<7 and base deficit >12 mmol/L).
• 2. Early onset severe or moderate neonatal encephalopathy in infants of
greater than 34 weeks of gestation. Cerebral palsy of the spastic
quadriplegic or dyskinetic type.
302

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ELBOHOTY152
303

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